Detection of metastasis of hepatocellular carcinoma (HCC) is crucial for early diagnosis. Epithelial-mesenchymal transition (EMT) is a common event in the metastasis of tumor cells. Slug and Snail are homologous proteins, which play an important role in EMT. The present study aimed to investigate whether Slug and Snail overexpression is associated with the invasiveness of HCC in vitro and in vivo. Invasion, colony formation and wound healing assays, as well as flow cytometry analysis, were performed to examine the invasiveness and proliferation capabilities of HepG2 cells following transfection with cNDA or the siRNA of Slug or Snail. The effects of Slug on HCC in vivo were examined using a xenograft model. Slug upregulation increased the percentage of cluster of differentiation (CD)133+ cells among HepG2 cells, and induced cell invasion and proliferation; whereas Snail upregulation did not affect the cells in vitro. The Slug overexpression group exhibited the highest rate of tumor growth compared with the Snail overexpression and control groups in vivo. These findings demonstrated that Slug increases the percentage of CD133+ cells, promotes the clonigenicity of HCC cells and induces a stronger stemness in Slug-overexpressing cells. These changes activate dormant developmental pathways in invading tumor cells. Thus, Slug may serve as a novel target for HCC prognosis and therapy.

Sex-determining region Y-related high mobility group box 4 (SOX4) has been proven to serve as a critical role in cancer development and progression. However, little is known about the pathological role of SOX4 in breast cancer patients. The purpose of this study is to measure the expression of SOX4 in breast cancer patients and to explore the clinical significance of SOX4. Using RT-PCR and Western blot, messenger RNA (mRNA) and protein expression of SOX4 were measured in breast cancer tissues and adjacent normal mammary tissues. The relationship of SOX4 expression with clinical characteristics of 148 breast cancer patients was analyzed by immunohistochemistry. In the present study, our results indicated that SOX4 mRNA and protein were highly expressed in breast cancer tissues compared with adjacent normal mammary tissues and positively correlated with clinical stage (I-II vs. III-IV; P = 0.008), T classification (T1-T2 vs. T3-T4; P = 0.013), N classification (N0-N1 vs. N2-N3; P < 0.001), M classification (M0 vs. M1; P = 0.001), estrogen receptor (negative vs. positive; P = 0.029), progesterone receptor (negative vs. positive; P = 0.004), and histological grade (G1 vs. G2-G3; P = 0.033) in breast cancer patients. Furthermore, we also found that SOX4 protein overexpression was an unfavorable prognostic factor in breast cancer patients (P < 0.001), regardless of clinical stage, tumor size, lymph node metastasis, and distant metastasis. Finally, high SOX4 expression was an independent poor prognostic factor for pancreatic patients through multivariate analysis (P = 0.033). In conclusion, SOX4 overexpression serves as an unfavorable prognostic biomarker in breast cancer patients.

We report for the first time elevated miR-29a expression in PBMCs of patients with ankylosing spondylitis, and miR-29a might be used as a useful diagnostic marker in new bone formation but cannot reflect disease activity.

Malignant melanoma, a tumor derived from melanocytes, shows severe drug resistance and prompt metastasis, causing a serious threat to human health. Circular RNAs (circRNAs) are widely expressed in mammals and have been indicated to play important roles in tumorigenesis. In the present study, we analyzed the variability of circRNAs in malignant melanoma by microarray and identified six differentially expressed circRNAs. In particular, we found that hsa_circ_0025039, which is formed by FOXM1 exons, is significantly upregulated in melanoma. In vitro, the knockdown of circ_0025039 inhibited cell proliferation, colony formation ability, invasion and glucose metabolism in melanoma cells. Additionally, we identified miR-198 as a direct target of hsa_circ_0025039. Furthermore, we demonstrated that hsa_circ_0025039 regulates CDK4 expression by sponging miR-198. In vivo study indicated that the silencing of hsa_circ_0025039 inhibits melanoma tumor formation and downregulates miR-198 and CDK4 expression. Taken together, our data showed that circ_0025039 promotes cell growth, invasion and glucose metabolism in malignant melanoma by sponging miR-198 and regulating CDK4.